28/3 Flashcards

1
Q

Safest antiepileptics to take in preg

A

lamotrigine, and carbamazepine mono
(although carbamazepine- cleft palate)

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2
Q

Sodium valproate congenital effect

A

neural tube defects
facial cleft
hypospadias

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3
Q

phenobarbital and phenytoin congenital effect

A

cardiac malformations
phenytoin - cleft palate

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4
Q

Predicting seizure deterioration in preg

A

seizure-free duration is the most important factor in assessing the risk of seizure deterioration.

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5
Q

how to test for ntd

A

Biochemical screening with maternal serum alphafetoprotein when combined with
ultrasonography increases the detection rate for neural tube defects to 94–100%,56 thereby
offering the opportunity to detect these abnormalities in early gestation for WWE.

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6
Q

What is the role of vitamin K in preventing haemorrhagic disease of the newborn and
maternal haemorrhage in WWE taking AEDs?

A

All babies born to WWE taking enzyme-inducing AEDs should be offered 1 mg of intramuscular
vitamin K to prevent haemorrhagic disease of the newborn.

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7
Q

enzyme inducing antiepileptics

A

phenytoin, carbamazepine, topiramate and phenobarbital,

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8
Q

BF and antiepileptics

A

Lamotrigine levetiracetam and topiramate transfer to
a larger extent in breast milk

Sodium valproate, carbamazepine, and phenytoin = minimal transfer.

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9
Q

non-enzyme-inducing AEDs

A

sodium valproate
levetiracetam
gabapentin
pregabalin

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10
Q

Lamotrigine

A

Effect on Lamo

CHC
May reduce lamotrigine effectiveness, requiring dose increase (up to two-fold) and serum level monitoring. Continuous CHC use advised to prevent fluctuations.

PO
Watch for lamotrigine toxicity signs (dizziness, ataxia, diplopia). Serum levels may need monitoring when stopping progestogen.

Contraceptive Effectiveness
CHC, POP and IMP may be less effective with lamotrigine—use additional contraception (e.g., condoms).
Depot , IUS, and IUDs unaffected.

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11
Q

AEDs and UKMEC

A

Enzyme-inducing
CHC 3
POP 3
PO-I 2
DMPA 1
IUD/ IUS 1
So same as any EI

Non enzyme inducing
CHC 1 (other than lamotrigine which is 3!!)
All rest 1
Unless teratogenic like –> Sodium valproate then only implant and coils

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12
Q

When does RPR become positive

A

Seroconversion 2-4 weeks after exposure
Treponemal Tests tend to become positive then

6 weeks

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13
Q

What are trep and non treps acc looking at

A

Treponemal Tests:
EIA and TPPA
Detect antibodies against the syphilis bacteria itself, and are generally more sensitive in early infection, remaining reactive indefinitely once positive.

> > Syphilis IgG (Syphilis EIA)
restest in 2 weeks if neg ulcer or high risk

Non-Treponemal Tests:
RPR
Detect antibodies against a substance produced by the body in response to the infection (reagin), and are used to monitor treatment response.
Less specific, and can be elevated due to other conditions, including autoimmune diseases or acute febrile illnesses.

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14
Q

STS TESTING
Biological False Positives:

A

If only one marker is positive within the range of syphilis screening tests this usually indicates a
false positive test. Discuss with Dr. The patient should be informed and asked to provide a
follow up sample 2 weeks later. If there is no change in the titre this confirms a false positive.

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15
Q

PN STS

A

In patients with primary syphilis all sexual partners in the past 3 months should be contacted. (50% of contacts of primary infection will also have syphilis)

In patients with secondary or early latent syphilis partner notification should include all
partners in the last 2 years.

Asymptomatic contacts of early syphilis should have serology performed at presentation + 4 and +12wks after last sexual contact with the index case.
(consider epidemiological treatment if unlikely to attend for FU)

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16
Q

STS FU post rx

A

Early
Rpt sereology following rx
+1month
+ 3,6 and 12 months
then 6 monthly until the RPR is negative or serofast.

RPR should fall by four-fold with in 3-6 / eight-fold with in 6-12 months. Normally comes neg.

15% of individuals with primary / secondary syphilis are expected to fail to show adequate serological response to treatment and may need further investigation.

Late
Falls is slower than above, and although it may
eventually become negative, it may also remain positive at low titre (<16).
Serological follow up is 6 monthly until serofast.

17
Q

Serology: early syphilis

A

An RPR >8 and a positive IgM suggest early, active syphilis.

18
Q

Penicillin desensitisation

A

BG: With the passage of time after a hypersensitivity reaction to Penicillin, most individuals cease to produce specific IgE and can safely be given the drug. About 10% of people however remain hypersensitive.

Penicillin V (Phenoxymethylpenicillin) given orally and increased by doubling the dose every 15 minutes for 14 doses.
The desensitisation procedure is performed in hospital with intravenous access and close personal medical supervision for 24 hours.

Mild cutaneous reactions are allowed to resolve spontaneously or are treated with Chlorphenamine
10 mg intravenously over one minute.

The injection of Benzathine Penicillin is then given within 30 minutes of completing the final dose of the desensitisation regimen, and the patient is
monitored overnight.

19
Q

false positive EIA vs RPR

A

EIA is generally more specific and less prone to false positives than RPR, especially when used in a reverse screening algorithm (EIA first, then RPR).

EAI false +ve: history of syphilis or other conditions that can cause a false-positive result.

RPR false +ve:
infections, autoimmune diseases, pregnancy, and certain medications.

20
Q

Syphilis IgG and IgM

A

IgM is detectable during the second week of infection, whereas production of IgG begins around the fourth week after infection and usually reaches much higher titres than those for IgM.

21
Q

Half life NO

A

5-10 seconds

22
Q

Half life RBC

23
Q

Half life GH

24
Q

Half life E2

A

2 hours
E2=2

25
Q

Half life E1

26
Q

Half life shbg

27
Q

Types of oestrogens

A

E1adipose
Estrone (ONE in the name)
Weakly active
Lowest number - menopause

E2 ovaries
Estradiol (DI)
biologically active, fetrtile yrs

E3 placenta
Estriol (TRI)
No biological activity

28
Q

Approach to delayed puberty in phenotypical females

A

Uterus (1mary)
Breast development (2nday)

YES uterus, NO breast development
Failure HPO axis before onset of puberty
Kallmans
Turners

YES uterus, YES breast development
Failure of HPO axis after breast developement
Ammenorhea at 15
PCOS,
Stress/ eating / exercise

NO uterus, YES breast development
Androgen insensitivity syndrome (AIS) (XY)
Müllerian agenesis (MRKH syndrome) (XX)

29
Q

MRKH

A

XX, 46
Assoc with WNT4

arrested development of the paramesonephric ducts at ~7 weeks after fertilisation.

N external genitalia
Normal growth and pubertal development
But reduced development of the uterus and upper two-thirds of the vagina –> ammenhorea (n ovaries)

Type I (MRKH): Characterized by uterine hypoplasia or aplasia, often with a rudimentary or absent vagina.

Type II (MURCS): A more severe form of MRKH, also known as MURCS association, involving Müllerian duct aplasia, renal agenesis, and cervicothoracic somite dysplasia.

ddx
(1) imperforate hymen, transverse vaginal septum, or cervical atresia.
(2) 46, XY DSDs: androgen insensitivity syndrome, CAH (CYP17A1, XY)

30
Q

Androgen Insensitivity Syndrome (AIS)

A

body is unable to respond normally to androgens

46,XY karyotype

Complete AIS (CAIS): Individuals have a female phenotype, with minimal or no pubic or axillary hair, and typically have a vagina but no uterus or fallopian tubes.

Partial AIS (PAIS): Individuals have variable phenotypes, ranging from ambiguous genitalia to a male phenotype with mild virilization.

Clinical Presentation: Primary amenorrhea.
May have a vagina but no uterus or fallopian tubes (in CAIS).
May have ambiguous genitalia or a male phenotype (in PAIS).
May have minimal or no pubic or axillary hair (in CAIS).

31
Q

classification of Müllerian anomalies

A

MUD B SAD

class I: uterine agenesis/uterine hypoplasia
Mullarian
Under/no development mul/parameso ducts (MRKH)
NONE

class II: unicornuate uterus/unicornis unicollis
Unicornuate
Only one Müllerian duct develops into a uterus, resulting in a single uterine horn.
ONE

class III: uterus didelphys,
Didelphys
2 separate uterus and two cervices.
Complete failure of the Müllerian ducts to fuse
FUSION

class IV: bicornuate uterus:
2nd most common type
Bicornuate
Heart-shaped appearance with a deep indentation or “horn” at the top
Incomplete fusion of the Müllerian ducts
FUSION

class V: septate uterus:
commonest and most symptomatic e.g RM
Septate
The uterus has a normal external shape, but the internal cavity is divided by a septum
Failure of the septum between the two fused Müllerian ducts to fully reabs
SEPTUM

class VI: arcuate uterus (7%)
less problems
Arcuate
The uterus has a slight indentation on the top, resembling a “dent” or “arc”.
Near-complete reabsorption of the uterovaginal septum, leaving a slight indentation.
SEPTUM

class VII: in utero diethylstilbestrol (DES) exposure (T-shaped uterus)
DES

32
Q

Contraception prolactinoma

A

Women with prolactinoma can use progestogen-only contraceptives.

Women with microprolactinoma (<10mm) can generally use combined hormonal contraceptives (≤30 μg
ethinylestradiol).

33
Q

Sympotms of prolactinoma

A

Menstrual disturbances (oligomenorrhoea, amenorrhoea)
Infertility
Galactorrhoea
Hypoestrogenism (e.g. vasomotor symptoms, dry vagina, etc)
Headache
Visual disturbance